Psychological Stress and Wound Healing in Humans

What We Know

Valentina S. Lucas, RN, MS, ANP-BC


Wounds. 2011;22(4):76-83. 

In This Article

The Stress Response

Often when we think of the stress response, we think of the "Fight or Flight" response, whereby stressful events trigger simultaneous activation of both the hypothalamic-pituitary-adrenal (HPA) axis in the central nervous system and the sympatho-adrenomedullary (SAM) axis in the sympathetic nervous system. Activation of the SAM axis stimulates the release of the catecholamines epinephrine and norepinephrine, leading to an increased heart rate, increased blood flow to skeletal muscles, and an elevation in glucose metabolism. The SAM pathway is faster and has a more immediate physiological effect. Activation of the SAM axis activates the inflammatory response.

Activation of the HPA axis activates the release of corticotrophin-releasing hormone (CRH) from the hypothalamus and CRH then stimulates the release of adrenocorticotropin (ACTH) from the anterior pituitary, which in turn triggers the release of the glucocorticoids from the adrenal glands. In humans, this glucocorticoid is cortisol. Normal levels of glucocorticoids are believed to be immunomodulatory. However, when stress increases levels of glucocorticoids, suppression of inflammatory and immune responses occur.[30] Cortisol has been shown to decrease circulating leukocytes and inhibit the migration of leukocytes to the site of injury or infection by decreasing capillary permeability and inhibiting chemotaxis. Elevated cortisol levels have been found to inhibit production of T cell-derived cytokines, such as interleukin 1.[4,31]


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